Gotowe bibliografie tematyczne / Hepatitis C virus

Gotowa bibliografia na temat „Hepatitis C virus”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 28 lipca 2024

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Artykuły w czasopismach na temat "Hepatitis C virus"

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Jamali, Ghulam Mustafa, Anwar Ali Jamali i Habibullah Shaikh. "HEPATITIS C VIRUS;". Professional Medical Journal 24, nr 11 (3.11.2017): 1621–29. http://dx.doi.org/10.29309/tpmj/2017.24.11.646.

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Objectives: The plan of this current research was in the direction for towards theassessment of the existing ELISA (Enzyme Linked Immunosorbant Assay) method throughantibodies testing for identification of hepatitis C virus disease by comparing their outcome withthe Real Time polymerase chain reaction analysis. Setting: Peoples Medical College HospitalNawabshah. Period: December 2015 to December 2016. Methods: In this current research 100blood samples were analyzed due to the presence of anti-HCV antibodies by 3rd-generationenzyme-linked immunosorbent assay testing. All the specimens were 100% positive. Polymerasechain reaction test was performed according to the laboratory directions in anti- hepatitis C virusantibodies positive patients to validate the diagnosis of hepatitis C virus infectivity. Results: Thisresearch shows that, the entire results were positive by Enzyme Linked Immunosorbant Assaytesting. As compared with polymerase chain reaction the of Enzyme Linked ImmunosorbantAssay in this research the screening test for anti hepatitis C virus - antibodies is about 2%false positive. Out of the 100 samples 98 cases are positive by Real Time polymerase chainreaction analysis while only 02 cases report are negative (2%). Conclusion: The proportion ofhepatitis C virus infectivity was 100% by 3rd-generation enzyme-linked immunosorbent assaytesting, 98% by Real Time polymerase chain reaction analysis. As in our research the hepatitisC virus –Ribonucleic acid is present in 98% cases who are the Anti- hepatitis C virus antibodiespositive patients, it can be suggested that Anti-HCV antibodies detection by third generationELISA technique in routine procedure is sufficient to determine HCV infection.
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AYGEN, Bilgehan, Mustafa Kemal ÇELEN, İftihar KÖKSAL, Selma TOSUN, Oğuz KARABAY, Tansu YAMAZHAN, Orhan YILDIZ, Celal AYAZ i Fehmi TABAK. "The Prevalence and Epidemiological Characteristics of Hepatitis B Virus and Hepatitis C Virus Coinfection in Turkey". Turkiye Klinikleri Journal of Medical Sciences 33, nr 5 (2013): 1245–49. http://dx.doi.org/10.5336/medsci.2012-32319.

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MD, Ian R. Mackay. "The new hepatitis virus: hepatitis C virus". Medical Journal of Australia 153, nr 5 (wrzesień 1990): 247–49. http://dx.doi.org/10.5694/j.1326-5377.1990.tb136892.x.

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Kim, Arthur. "Hepatitis C Virus". Annals of Internal Medicine 165, nr 5 (6.09.2016): ITC33. http://dx.doi.org/10.7326/aitc201609060.

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Kaplan, David E. "Hepatitis C Virus". Annals of Internal Medicine 173, nr 5 (1.09.2020): ITC33—ITC48. http://dx.doi.org/10.7326/aitc202009010.

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NAQVI, S. M. ABBAS, Muhammad Shiraz Khan, QURBAN ALI KHASKHELI, Muhammad Saeed Talpur i SHAHID HABIB ANSARI. "HEPATITIS C VIRUS". Professional Medical Journal 13, nr 04 (16.12.2006): 604–7. http://dx.doi.org/10.29309/tpmj/2006.13.04.4935.

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`To find out the prevalence of antibody to HCV in serum of blood donorpopulation in our Community (Karachi). To estimate level of serum ALT in blood donors as possible marker of liverinfectivity and hence increasing awareness among the people about the prevention and spread of HCV in Communityand to give suggestions in the formulation of blood transfusion policies. Setting: At Microbiology Department, BasicMedical Sciences Institute, Jinnah Postgraduate Medical Centre Karachi. Period: From September 2001 to January2002. Material and Methods: 150 subjects, consisting of volunteer blood donors and 50 subjects selected from healthypopulation who had never received or donated blood. Results: Among 150 blood donors, 07 subjects (4.66%) werefound to be anti HCV positive. Mean age of anti HCV positive donors was 32.85±7.35 years with male predominance.Conclusion: It is concluded that HCV is notorious for its infectivity, chronocity and complications. Hence HCV spreadshould be controlled by screening blood donors for anti HCV antibodies and observing Universal rules in medicalpractice.
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Dana, Franklin, Paul R. Becherer i Bruce R. Bacon. "Hepatitis C virus". Postgraduate Medicine 95, nr 6 (czerwiec 1994): 121–30. http://dx.doi.org/10.1080/00325481.1994.11945847.

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Klevens, R. Monina, i Anne C. Moorman. "Hepatitis C virus". Journal of the American Dental Association 144, nr 12 (grudzień 2013): 1340–47. http://dx.doi.org/10.14219/jada.archive.2013.0069.

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Ye, Jin. "Hepatitis C Virus". Arteriosclerosis, Thrombosis, and Vascular Biology 32, nr 5 (maj 2012): 1099–103. http://dx.doi.org/10.1161/atvbaha.111.241448.

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Jadoul, Michel, Alberto Frosi, MariaClotilde Ragni, Leonardo Salvaggio, Silvia Vezzoli, Francesco Vezzoli, Medhat Darwish i in. "Hepatitis C virus". Lancet 345, nr 8943 (styczeń 1995): 189–91. http://dx.doi.org/10.1016/s0140-6736(95)90192-2.

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Rozprawy doktorskie na temat "Hepatitis C virus"

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Berg, Thomas. "Chronische Hepatitis C". Doctoral thesis, Humboldt-Universität zu Berlin, Medizinische Fakultät - Universitätsklinikum Charité, 2002. http://dx.doi.org/10.18452/13812.

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Die vorliegende Habilitationsschrift befasst sich schwerpunktmäßig vor allem mit der Klinik und Therapie der Hepatitis C. Evaluiert wurden: 1. verschiedene therapeutische Strategien, 2. die Ursachen der "Non-Response" auf eine anti-virale Therapie sowie 3. die klinische Relevanz der neu entdeckten Hepatitis-assoziierten Viren und 4. ihre Bedeutung bei Patienten mit akuter bzw. chronischer Lebererkrankung unklarer Ätiologie sowie bei Patienten vor und nach Lebertransplantation. Ad 1. Aus dem Vergleich verschiedener Therapie-Konzepte wie der Kurzzeit- Kombinationstherapie, Triple-Therapie, Hochdosis-Interferon?-Therapie und der Anwendung antiviraler Substanzen wie Ribavirin und Amantadin ergaben sich neue Erkenntnisse hinsichtlich relevanter prognostischer Parameter für die Therapieresponse. Ad 2. Analysiert wurden die möglichen molekularen Mechanismen der Therapieresponse bzw. Non-Response sowie der Stellenwert von Interaktionen bestimmter HCV-Proteine (NS5A, E2, sogenannte PKR-eIF2a Phosphorylisations-Homologie-Domäne [PePHD]) mit den Interferon? induzierten Effektorproteinen. Es konnte gezeigt werden, daß die Anzahl der Mutationen innerhalb des NS5A Proteins einen prognostischen Parameter darstellen hinsichtlich der Response auf eine Interferon?-Therapie. Dagegen spielen Mutationen innerhalb der PePHD-Region keine Rolle. Ad 3. Aus den Untersuchungen zur klinischen Relevanz der neu entdeckten Hepatitis-assoziierten Viren GB Virus-C/Hepatitis G Virus (GBV-C/HGV) und TT-Virus (TTV) ergaben sich keine Hinweise bzgl. eines Einflusses von GBV-C/HGV bzw. TTV-Infektionen auf den Verlauf der chronischen Hepatitis C. Die durchgeführten Verlaufsuntersuchungen bei koinfizierten Patienten sprechen dafür, daß es sich um Interferon-sensitive Viren handelt; jedenfalls beeinflussen sie nicht die IFN?-induzierte Response. Ad 4. Untersucht wurden ferner die Prävalenz, Transmission und Relevanz der GBV-C/HGV und TTV-Infektion im Hinblick auf ihre Hepatitis-induzierenden Eigenschaften. Die Ergebnisse belegen, dass beide Viren parenteral übertragen werden, und dass sie eine hohe Prävalenz bei Patienten mit parenteralen Risikofaktoren besitzen. Eine Hepatitis-induzierende Potenz dieser Viren konnten wir nicht beobachten; bei der Mehrzahl aller chronisch infizierter Personen ließen sich keine Zeichen einer chronischen Hepatitis finden.
The major goal of this thesis is the analysis of the clinical outcome of patients with Hepatitis C virus (HCV) infection and the response to therapy. Analysed were 1. different types of therapeutic strategies 2. causes responsible for ineffective antiviral therapy (non-response) 3. clinical relevance of the newly discovered hepatitis-associated viruses and 4. the role of these viruses in patients with acute or chronic hepatitis of unknown causes and in those receiving liver grafts. Ad 1. Compared were different therapeutic concepts such as short-term combination therapy, triple-therapy, high dose IFN?-therapy and the use of antiviral substances such as ribavirin and amantadine. It emerged that relevant prognostic parameters can be deduced with respect to the therapeutic response rate. Ad 2. Analysed were possible molecular mechanisms, which may interfere with response or non-response to antiviral therapy. In this respect, we focussed on the interaction of certain HCV-proteins as NS5A, E2, so-called PKR-eIF2a phosphorylisation-homology-domain (PePHD). with the interferon-?-induced effector proteins. There is evidence, that number of mutations within the NS5A proteins are of prognostic relevance with respect to the response to interferon?-therapy. In contrast, mutations within the PePHD-region do not play any role in this respect. Ad 3. We also studied the clinical relevance of the newly discovered viruses GBV-C/HGV and TTV, and found, that they have no impact concerning the course of chronic hepatitis C. These viruses are interferon-sensitive and do not influence the IFNa-response as it could be documented by following the course of co-infected patients. Ad 4. Our studies also focused on the prevalence, transmission and relevance of GBV-C/HGV and TTV infections with respect to their role as hepatitis-inducing agents. We can show that both virus types are parenterally transmitted. There is a high prevalence for both types in patients confronted with risk factors for parenteral factors. From analysis of many patients being chronically infected with these viruses it became quite clear that they lack any important potency to provoke chronic liver disease.
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Roy, Kirsty McLiver. "Hepatitis C virus in saliva". Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297005.

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Buckton, Andrew John. "Multitypic hepatitis C virus infection". Thesis, Open University, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.435903.

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Mohamed, Gibrial Saleh. "Hepatitis C virus infection in Libya". Thesis, King's College London (University of London), 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.518840.

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Shen, Hong. "Hepatitis C infection models". Thesis, Paris 5, 2012. http://www.theses.fr/2012PA05T016.

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L'hépatite C (VHC) est l'une des causes principales de maladies du foie dans le monde, qui représentent un risque élevé d'évoluer vers la cirrhose et le carcinome hépatocellulaire. Actuellement, le traitement standard de l’infection par le VHC est l'interféron pégylé-(peg-IFN) et la ribavirine. Bien que le taux de la réponse virale soutenue (RVS) au traitement se soit améliorée au cours de ces années, cette thérapie n'est pas efficace chez tous les patients. En outre, plusieurs effets secondaires toxiques, de complications et le coût élevé limitent la compliance du patient et l'efficacité du traitement. Il n'existe pas de modèle simple d'infection par le VHC et il est nécessaire de développer des modèles in vitro et in vivo utiles pour étudier la physiopathologie de l'infection par le VHC, y compris les événements précoces de l'infection aiguë (l'entrée du virus, des mécanismes immunologiques et génétiques prédictifs) ainsi que l'évaluation de la puissance des médicaments antiviraux contre le VHC. Nous rapportons ici, nos efforts visant à développer des modèles appropriés de l'infection par le VHC. Dans un premier temps, nous avons établi un modèle de petit animal pour étudier l'infection par le VHC. Tupaia est un petit animal, apparenté aux primates et peu couteux. Dans notre travail, nous avons étudié la susceptibilité du tupaia à l'infection par VHC. Douze tupaias adultes ont été inoculés avec le VHC provenant de sérum de patient et d'ARN du VHC (génotype 1a). Trois jeunes tupaias ont été artificiellement nourris pendant un mois et ensuite inoculés par le VHC provenant de sérum du patient. L'ARN du VHC, les anticorps anti-VHC et l’évolution des quasi-espèces du VHC ont été déterminées chez l'animal avant et après l'inoculation. L'infection transitoire et intermittente s'est produite chez deux des 3 jeunes tupaias et l’infection chronique par le VHC s’est produite chez quatre tupaias sur 12 tupaias adultes. Le tupaia devrait représenter un modèle utile pour l'étude de l’infection chronique par le VHC. Dans une deuxième étape, un système de culture in vitro d'hépatocytes primaires de Tupaia a été établi, dans lequel l'infection par le VHC ne pouvait être bloquée ni par le CD81 soluble ni par des anticorps dirigés contre le CD81. Pour comprendre ces résultats, nous avons cloné, séquencé la grande boucle extracellulaire (LEL) du CD81 chez le Tupaia et analysé l'interaction de la protéine d’enveloppe E2 du VHC avec la LEL du CD81 chez le Tupaia par un test « enzyme-linked immunosorbent assay » (EIA). Nous avons constaté que chez le Tupaia, la séquence d'acides aminés du LEL de CD81 qui se lie au VHC présentait en 6 résidus d'acides aminés différents par rapport à la séquence humaine et la capacité de LEL de CD81 à se lier à la proteine d’enveloppe E2 du VHC a également diminuée. La structure différente de CD81 chez l’homme et chez le tupaia pourrait expliquer l'altération de l'interaction entre CD81 et la proteine E2 du VHC. Ce résultat démontre un rôle important de LEL du CD81 pour l'entrée du VHC. Dans une troisième étape, nous avons développé un modèle ex vivo de culture de tranches de foie humain et leur infection par le VHC. Le développement de lignées cellulaires provenant d’hepatocarcinome, permissives à la réplication du VHC, a fourni d'importants nouveaux outils virologiques pour étudier les mécanismes de l'infection par le VHC, mais ce modèle expérimental reste relativement éloigné des conditions physiologiques et pathologiques. Nous rapportons ici le développement d'un nouveau modèle ex vivo utilisant la culture de tranches de foie humain adulte, démontrant, pour la première fois, la capacité d’isolats primaires ainsi que JFH -1, H77/C3, Con1/C3 (HCVcc), de répliquer et de produire de novo des particules virales infectieuses ayant un titre viral élevé…
Hepatitis C virus (HCV) is one of the major causes of liver disease all over the world which has a high risk to progress to cirrhosis and hepatocellular carcinoma. Currently, the licensed standard treatment of HCV infection is Pegylated-interferon (peg-IFN) and ribavirin. Although the sustained viral response (SVR) rate of treatment has improved during these years, this therapy is not effective in all patients. In addition, several toxic side effects, complication and high cost limit the patient compliance and the efficacy of the treatment. There is no easy model of HCV infection and it is necessary to develop useful in vitro and in vivo models to study the pathobiology of HCV infection, including early events of acute infection (viral entry, immunological mechanisms, and genetic predictors) as well as the evaluation of the potency of the HCV antiviral drugs. We report here in our efforts in developing suitable models of HCV infection. In a first step, we preliminary established a small animal model to study HCV infection. Tupaia is a small, closed related to primate and cost-effective animal. In our work, we investigated the susceptibly of tupaia to HCV infection. Twelve adult tupaias were inoculated with native HCV from patient serum and full-length HCV RNA (Genotype 1a). Three young tupaias were artificially breeded for a month and then inoculated by native HCV from patient serum. HCV RNA, anti-HCV and HCV quasi species evolution were determined in the animal before and after inoculation. Transient and intermittent infection occurred in two among 3 young tupaias and HCV chronic infection occurred in four among 12 adult tupaias. Tupaia should represent a useful model for study HCV chronic infection. In a second step, an in vitro culture system of primary tupaia hepatocytes has been established in which HCV infection could be blocked neither by the soluble CD81 nor by antibodies against CD81. To understand these results, we cloned, sequenced the large extracellular loop (LEL) of tupaia CD81 and analyzed the interaction of HCV E2 with the tupaia CD81 LEL by enzyme-linked immunosorbent assay (EIA). We found that in the tupaia the amino acids sequence of HCV CD81 LEL presented in 6 different amino acid residues compared with human CD81 LEL sequence and the CD81 LEL ability to bind to HCV E2 was also decreased. The different structure of CD81 between human and tupaia could explain the alteration of the interaction between HCV E2 and CD81. This result demonstrated an important role of CD81 LEL for HCV entry. In a third step, we developed an ex vivo model of human liver slices culture and their infection with HCV. The development of human cultured HCV-replication-permissive hepatocarcinoma cell lines has provided important new virological tools to study the mechanisms of HCV infection; however this experimental model remains distantly related to physiological and pathological conditions. Here, we report the development of a new ex vivo model using human adult liver slices culture, demonstrating, for the first time, the ability of primary isolates to undergo de novo viral replication with the production of high titer infectious virus, as well as JFH-1, H77/C3, Con1/C3 (HCVcc). This experimental model was validated by demonstrating the HCV neutralization or HCV inhibition, in a dose-dependent manner, either by CD81 or E2 specific antibodies or convalescent serum from a recovered HCV patient, or by anti-viral drugs. This new ex vivo model represents a powerful tool for studying the viral life cycle, dynamics of virus spread in the liver and also for evaluating the efficacy of the new antiviral drugs. In the last step, we evaluated the efficacy of the new antiviral drugs with our ex vivo model of human adult liver slices. HCV NS3/4A protease is essential for viral replication and has been one of the most important target for developing specific antiviral drug
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Pajenčkovskytė, Karolina. "Sergančiųjų lėtiniu virusiniu C hepatitu genotipai". Master's thesis, Lithuanian Academic Libraries Network (LABT), 2004. http://vddb.library.lt/obj/LT-eLABa-0001:E.02~2004~D_20040608_165139-44050.

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Cramer, Janina. "Funktionelle Charakterisierung der RNA-abhängigen RNA-Polymerase des Hepatitis-C-Virus Untersuchung molekularer Mechanismen der Substratspezifität von DNA-abhängigen DNA-Polymerasen /". [S.l. : s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=971700796.

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Christie, John Michael Landale. "Viral persistence in hepatitis C virus infection". Thesis, University of Southampton, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268465.

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Jones, Louisa Alice School of Biotechnology And Biomolecular Sciences UNSW. "Aptamers to the hepatitis C virus polymerase". Awarded by:University of New South Wales. School of Biotechnology And Biomolecular Sciences, 2005. http://handle.unsw.edu.au/1959.4/32734.

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Treatments for the hepatitis C virus (HCV) are currently only partially effective. Research into antivirals directed at HCV viral proteins are commonly based and tested on a single genotype, namely genotype 1. This is despite the high level of variability of the RNA virus and the frequency of infection with genotypes other than 1. The systematic evolution of ligands by exponential enrichment (SELEX) is a novel in vitro approach for the isolation of antiviral agents. SELEX allows rapid screening of vast nucleic acid libraries to isolate sequences (termed aptamers) that bind to target proteins with high affinity. The SELEX approach was used in the present study to isolate DNA aptamers to the RNAdependent RNA polymerase (RdRp) [non-structural protein B (NS5B)] protein of HCV subtype 3a, with the aim of inhibiting polymerase activity. Ten rounds of selection were performed using a Biacore 2000 and resultant aptamers cloned from rounds 2, 4, 8 and 10. Sequences of aptamers were aligned to elucidate common motifs and a proportion of the aptamers from rounds 8 and 10 (29/48) were screened for binding ability using the Biacore. The five ???best binding??? aptamers were investigated for inhibition of 3a polymerase activity in an in vitro polymerase assay. Two aptamers, r10/43 and r10/47, were chosen for further studies based on their ability to inhibit polymerase activity. The inhibition constants (Ki) of r10/43 and r10/47 were estimated to be 1.4 + 2.4 nM and 6.0 + 2.3 nM respectively. The affinity (Kd) of these aptamers for the 3a polymerase was estimated to be 1.3 + 0.3 nM (r10/43) and 23.5 + 6.7 nM (r10/47). The estimated inhibition and dissociation constants of these two aptamers are among the best for inhibitory aptamers of the HCV enzymes (polymerase and protease). Inhibition of HCV 3a polymerase appeared to be specific for r10/47, whilst r10/43 also had some inhibitory effect on norovirus and ??6 polymerase activity. This study is the first description of an inhibitor to the HCV subtype 3a polymerase that investigates genotypic specificity of targeted antivirals.
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Post, Jeffrey John Medical Sciences Faculty of Medicine UNSW. "Primary hepatitis C virus infection in prisons". Awarded by:University of New South Wales. Medical Sciences, 2008. http://handle.unsw.edu.au/1959.4/41511.

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Infection with hepatitis C virus (HCV) causes significant morbidity and mortality. An understanding of the factors associated with both acquisition and clearance of HCV infection is critical to prevention strategies including vaccine development. Although research in the prison environment is logistically challenging, inmates are a premier risk group. Accordingly, a prospective cohort study of prisoners with monthly sampling for HCV viraemia was undertaken to assess the incidence of, and risk factors for, infection; and to assess the natural history of infection when detected by viraemia. The incidence of infection was 8 per 100 person years, with the incidence of "high risk" and "possible" HCV transmission risk events being 61 and 210 per 100 person years respectively. The first case of HCV infection in prison with tattooing as the probable route of acquisition was reported. A novel phenotype of HCV infection with HCV viraemia and subsequent clearance without the development of symptoms, biochemical hepatitis or seroconversion on HCV specific enzyme immunoassay (EIA), despite more than one year of follow-up, was reported. HCV-specific cell mediated immune responses were detected in the subjects analysed. These subjects also had indeterminate HCV serological responses directed against non-structural proteins detected on a recombinant immunob10t assay (RIBA) that were stable over time and typically predated HCV viraemia. The prevalence of such responses ranged from 29-79% in other relevant cohorts, including injecting drug users (IDUs) and multiply-transfused patients with thalassaemia. The antibody response against the non-structural protein, NS5 was the most reproducible. This reactivity was blocked in 57% of subjects when sera were pre-incubated with recombinant HCV proteins, suggesting HCV-specificity. A case-control study was undertaken to examine whether such responses predicted protection from "classical" HCV infection with EIA seroconversion. Cases that developed HCV viraemia and EIA seroconversion were more likely to have these responses at baseline (when aviraemic) than controls, demonstrating that they do not protect against acute infection. However, the rate of viral clearance in subjects with indeterminate RIBA responses that subsequently developed acute infection and were followed for viral clearance was high (88%), suggesting that such subjects have immune responses that are associated with viral clearance.
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Książki na temat "Hepatitis C virus"

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W, Reesink H., red. Hepatitis C virus. Basel: Karger, 1994.

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W, Reesink H., red. Hepatitis C virus. Wyd. 2. Basel: Karger, 1998.

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Shiffman, Mitchell L., red. Chronic Hepatitis C Virus. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-1192-5.

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Law, Mansun, red. Hepatitis C Virus Protocols. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8976-8.

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Jirillo, Emilio, red. Hepatitis C Virus Disease. New York, NY: Springer New York, 2008. http://dx.doi.org/10.1007/978-0-387-71376-2.

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Miyamura, Tatsuo, Stanley M. Lemon, Christopher M. Walker i Takaji Wakita, red. Hepatitis C Virus I. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56098-2.

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Miyamura, Tatsuo, Stanley M. Lemon, Christopher M. Walker i Takaji Wakita, red. Hepatitis C Virus II. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-56101-9.

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Chayama, Kazuaki, red. Hepatitis C Virus Treatment. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-2416-0.

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Sawyer, Forrest. Hepatitis C. Princeton, N.J: Films for the Humanities & Sciences, 2003.

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Berenguer, Marina, red. Hepatitis C Virus and Liver Transplantation. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-8438-7.

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Części książek na temat "Hepatitis C virus"

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Bendinelli, Mauro, Maria Linda Vatteroni, Fabrizio Maggi i Mauro Pistello. "Hepatitis C Virus". W Viral Hepatitis, 65–127. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-702-4_4.

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Caselmann, Wolfgang H. "Hepatitis C Virus". W Encyclopedia of Cancer, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_2661-2.

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Tedbury, Philip, i Mark Harris. "Hepatitis C Virus". W Viral Proteases and Antiviral Protease Inhibitor Therapy, 47–69. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-90-481-2348-3_3.

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Bowden, Scott. "Hepatitis C Virus". W PCR for Clinical Microbiology, 253–56. Dordrecht: Springer Netherlands, 2010. http://dx.doi.org/10.1007/978-90-481-9039-3_37.

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Caselmann, Wolfgang H. "Hepatitis C Virus". W Encyclopedia of Cancer, 2034–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_2661.

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Caselmann, Wolfgang H. "Hepatitis C Virus". W Encyclopedia of Cancer, 1665–67. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_2661.

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van Balen, J. A. M., A. A. Demeulemeester, M. Frölich, K. Mohrmann, L. M. Harms, W. C. H. van Helden, L. J. Mostert i J. H. M. Souverijn. "Hepatitis C virus". W Memoboek, 129–30. Houten: Bohn Stafleu van Loghum, 2012. http://dx.doi.org/10.1007/978-90-313-9129-5_69.

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Wong, David K. H., i Bruce D. Walker. "Hepatitis C Virus". W Human Tumor Viruses, 301–29. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555818289.ch10.

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Mallory, Melanie, i David Hillyard. "Hepatitis C Virus". W Clinical Virology Manual, 351–61. Washington, DC, USA: ASM Press, 2016. http://dx.doi.org/10.1128/9781555819156.ch25.

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Koh, Christopher, Qisheng Li i Jake Liang. "Hepatitis C Virus". W Clinical Virology, 1313–45. Washington, DC, USA: ASM Press, 2016. http://dx.doi.org/10.1128/9781555819439.ch54.

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Streszczenia konferencji na temat "Hepatitis C virus"

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Eid, Fatma Elzahraa, Haitham Elmarakeby, Lenwood Heath i Mahmoud ElHefnawi. "Human microRNAs targeting hepatitis C virus". W 2014 Middle East Conference on Biomedical Engineering (MECBME). IEEE, 2014. http://dx.doi.org/10.1109/mecbme.2014.6783236.

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Gür, A., M. Karakoç, MF Geyik, K. Nas, R. Çevik, AJ Saraç, S. Em i F. Erdogan. "SAT0135 Association between hepatitis c virus antibody, hepatitis b virus antigen and fibromiyalgia". W Annual European Congress of Rheumatology, Annals of the rheumatic diseases ARD July 2001. BMJ Publishing Group Ltd and European League Against Rheumatism, 2001. http://dx.doi.org/10.1136/annrheumdis-2001.594.

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Twu, WI, K. Tabata, D. Paul i R. Bartenschlager. "Role of autophagy in hepatitis C virus replication". W 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677294.

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Campo, David S., Zoya Dimitrova, Pavel Skums i Yury Khudyakov. "Mutational robustness of hepatitis C virus intra-host variants". W 2013 IEEE 3rd International Conference on Computational Advances in Bio and Medical Sciences (ICCABS). IEEE, 2013. http://dx.doi.org/10.1109/iccabs.2013.6629229.

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Keval, Ram. "Dynamics of Hepatitis C Virus with Saturation Incidence Rate". W 2nd Annual International Conference on Computational Mathematics, Computational Geometry & Statistics. Global Science Technology Forum, 2013. http://dx.doi.org/10.5176/2251-1911_cmcgs13.47.

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Kaushik, Vikas, Joginder Singh i Nidhi Sharma. "In silico peptide based vaccine against hepatitis C virus". W 2016 International Conference on Bioinformatics and Systems Biology (BSB). IEEE, 2016. http://dx.doi.org/10.1109/bsb.2016.7552119.

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Lin, Yu-Cheng, Ming-Yuan Huang, Kung-Chia Young, Ting-Tsung Chang i Ching-Yi Wu. "Rapid micro-PCR system for hepatitis C virus amplification". W Micromachining and Microfabrication, redaktorzy Eric Peeters i Oliver Paul. SPIE, 2000. http://dx.doi.org/10.1117/12.395627.

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KRISHNAMOORTHI, RAJESH, Palaniappan Manickam, Rajeev Sudhakar, Ankit Rathod, Arun Muthuswamy i Teena Chopra. "Impact Of Hepatitis C Virus Seropositivity In Lung Transplantation". W American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4022.

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Fraga Bueno, E., A. Casás Martínez i I. Rodríguez Penín. "4CPS-089 Current status of hepatitis C virus infection". W 27th EAHP Congress, Lisbon, Portugal, 22-23-24 March 2023. British Medical Journal Publishing Group, 2023. http://dx.doi.org/10.1136/ejhpharm-2023-eahp.110.

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Guo, Tailin. "The bioinformatics analysis of hepatitis C virus E2 protein". W International Conference on Intelligent Systems and Knowledge Engineering 2007. Paris, France: Atlantis Press, 2007. http://dx.doi.org/10.2991/iske.2007.131.

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Raporty organizacyjne na temat "Hepatitis C virus"

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Sjogren, Maria H., i Kent Holtzmuller. Hepatitis C Virus Infection: Mechanism of Disease Progression. Fort Belvoir, VA: Defense Technical Information Center, październik 2001. http://dx.doi.org/10.21236/ada406083.

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Sjogren, Maria H. Hepatitis C. Virus Infection: Mechanism of Disease Progression. Fort Belvoir, VA: Defense Technical Information Center, październik 2004. http://dx.doi.org/10.21236/ada433067.

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Sjogren, Maria H., i Brooke Huntley. Hepatitis C. Virus Infection: Mechanisms of Disease Progression. Fort Belvoir, VA: Defense Technical Information Center, październik 2007. http://dx.doi.org/10.21236/ada477987.

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Koizumi, Yoshiki, Syo Nakajim, Hirofumi Ohash, Yasuhito Tanaka, Takaji Wakita, Alan S. Perelson, Shingo Iwami i Koichi Watashi. Quantifying antiviral activity optimizes drug combinations against hepatitis C virus infection. Office of Scientific and Technical Information (OSTI), marzec 2016. http://dx.doi.org/10.2172/1242919.

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Nelson, David, Michael Fried, Mark Sulkowski, Donna Evon, Jodi Segal, Anna Lok, Paul Stewart_ Stewart i in. Comparing Oral Medicines to Treat Hepatitis C Virus -- The PRIORITIZE Study. Patient-Centered Outcomes Research Institute® (PCORI), marzec 2022. http://dx.doi.org/10.25302/03.2022.hpc.150327891.

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Ely, Danielle, i Gregory Elizabeth C.W. Trends and Characteristics in Maternal Hepatitis C Virus Infection Rates During Pregnancy: United States, 2016–2021. National Center for Health Statistics (U.S.), kwiecień 2023. http://dx.doi.org/10.15620/cdc:124659.

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This report presents data on trends for hepatitis C virus infection among mothers giving birth in the United States from 2016 through 2021, and rates by selected maternal characteristics for 2016, 2020, and 2021.
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Lyons, Megan, Thomas Bennett, Felicia Gray-Hamilton i Margaret Harvey. Hepatitis C Virus Screening Strategies to Improve Early Identification and Treatment: ​ A Scoping Review​. University of Tennessee Health Science Center, kwiecień 2023. http://dx.doi.org/10.21007/con.dnp.2023.0046.

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Litwin, Alain. Patient-Centered Hepatitis C Virus Care for People Who Inject Drugs -- The HERO Study. Patient-Centered Outcomes Research Institute (PCORI), maj 2024. http://dx.doi.org/10.25302/05.2024.hpc.150328122ic.

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Martinez-Chantar, Malu. Especial Premio Nobel de Medicina 2020: La ciencia vence al virus de la hepatitis C. Sociedad Española de Bioquímica y Biología Molecular, październik 2020. http://dx.doi.org/10.18567/sebbmdiv_rpc.2020.10.1.

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Terzieva, Kalina, Metody Kunchev, Hristina Hitkova, Tzetza Doichinova, Tanya Petkova, Krasimira Mekoushinov i Dimitar Shalamanov. Molecular-genetic Indicators as Part of an Epidemiologic Study on Patients with Virus Hepatitis C. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, kwiecień 2021. http://dx.doi.org/10.7546/crabs.2021.04.15.

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